The dopamine-containing neurons of the midbrain have been implicated in a broad array of psychiatric disorders, ranging from schizophrenia to drug abuse and depression. However, studies seem to indicate that it is not the dopamine neurons themselves that are responsible for these pathological states, but instead the disorders appear to arise due to a disruption of dopamine neuron regulation by afferent inputs. Dopamine neurons recorded in vivo are known to exhibit multiple functional activity states, including baseline tonic firing and phasic activation in response to salient stimuli. Phasic burst firing is believed to be the behaviorally relevant “signal” of the dopamine neuron, whereas the level of tonic discharge represents the “gain” or the level of amplification of this signal. This tonic gain is differentially regulated by multiple brain regions, including the hippocampus, the amygdala, and the prefrontal cortex. Disruptions in these regions can interfere with the normal tonic/phasic balance within the dopamine system. Electrophysiological and behavioral studies in animal models of psychiatric disorders, as well as and human imaging studies in patients, suggest that this disruption may underlie the pathological state of the dopamine system that is present in psychiatric disorders. Specifically, we found that hippocampal hyperactivity in schizophrenia may be responsible for the hyperdopaminergic state of psychosis, whereas prefrontal cortical-amygdala overdrive diminishes reward-related dopamine neuron activity leading to anhedonia in depression. This type of information can contribute both to a better understanding of the pathophysiology of major psychiatric disorders, as well as glean insights into novel avenues of treatment and potentially in preventing the emergence of these disorders.

The dorsal anterior cingulate cortex (dACC), orbitofrontal cortex (OFC), ventrolateral and ventromedial prefrontal cortex (vlPFC, vmPFC) and their connections with the basal ganglia play a central role in reward and decision-making. These areas, along with their white matter pathways, are closely associated with several psychiatric disorders, including depression, obsessive–compulsive disorder (OCD), and addiction. While their connections define the reward-related cortical and basal ganglia regions, their terminals also interface in specific locations with those from cognitive control cortical areas. These regions, specifically located in the dACC, vlPFC, and striatum, are in pivotal positions for providing a ‘platform’ for bottom-up and/or top down control of goal directed behaviors. The first part of this talk will address the connectivity of the reward circuit and its interface with cognitive control cortical regions. Axons from reward-related and cognitive control cortical areas travel through several white matter bundles, that shows changes in volume and diffusivity in several psychiatric disorders. Importantly, these WM bundles are targets for invasive surgeries for treatment of depression and OCD, including lesions and deep brain stimulation (DBS). For example, anterior capsulotomy and DBS, two surgical treatments for OCD and depression, target the internal capsule. Lesions of the dorsal cingulum bundle (cingulotomy), is also a target for depression and OCD, and the subgenual cingulum bundle is a DBS target for depression. The second part of this talk will demonstrate the PFC fiber positions through these bundles demonstrating the likely connections captured at the three surgical targets.

The Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative has the ambitious goal of elucidating how neuronal ensembles interactively encode higher brain processes. To accomplish this goal, new and improved methods for both recording and manipulating neuronal activity will be needed. In this thal, I will focus on technologies for manipulating neuronal activity. In particular I will present an enhanced chemogenetic toolbox that allows non-invasive, multiplexed spatiotemporal control of neuronal activity in domains ranging from single synapses to ensembles of neurons.

Schizophrenia is a severe psychiatric disorder affecting 1% of the world’s population, leading to high human, social and economic burdens. Understanding how the interaction of gene and environment risk factors during neurodevelopment leads to cognitive, affective and social impairment is a central challenge in schizophrenia pathophysiology. I will discuss how these risk factors converge on a hub composed of NMDA-receptor hypofunction, neuroinflammation and redox imbalance/oxidative stress, leading to structural and functional dysconnectivity. Based on oxidative stress markers and genetic associations in patients, this hypothesis received support from a glutathione deficit preclinical model (gclm -/-mice), reproducing numerous schizophrenia phenotypes including NMDA receptor hypofunction, inflammation, impaired parvalbumine fast-spiking GABA interneurons (PVI), myelination, neural synchronization and behavioral anomalies. This model also highlights childhood and peripuberty as critical periods of high vulnerability for environmental adverse insults. Indeed, additional oxidative challenges in juvenile and peripubertal ages, but not in adult gclm-/- mice, lead to severe and permanent PVI impairment. Regulation of redox state in PVI also balances plasticity and stability across cortical development, through delaying and/or keeping critical periods of plasticity open-ended. Moreover, long range connections may also be affected by redox dysregulation during development: gclm-/- mice present myelin marker deficits in the prefrontal cortex at peripuberty, involving the Fyn kinase pathway dysregulation, which lead to decreased oligodendrocyte proliferation. Most importantly, the antioxidant and GSH precursor N-acetyl-cysteine (NAC), prevents the morphological, biochemical, physiological and behavioral alterations described above. A translational approach towards prevention attempts to modify the disease course by redox modulators will be presented.

The hippocampal formation is one of the most extensively studied regions of the brain, with well described anatomy and basic physiology; moreover, aspects of human memory mediated by hippocampus are well characterized. In schizophrenia, alterations in hippocampal anatomy, perfusion and activation are consistently reported; impairments in declarative memory function, especially in the flexible use of event memories (e.g., in the service of memory-based inference), are common. Postmortem molecular changes suggest a selective reduction in glutamate transmission in the dentate gyrus (DG) and in its efferent fibers, the mossy fiber pathway. A reduction in DG glutamatergic output and in its information processing functions could generate two co-occurring outcomes in hippocampus: (a) a change in homeostatic plasticity processes in CA3, accompanied by increased activity due to reduced afferent stimulation from DG onto CA3 neurons, a process that could increase the ‘pattern completion’ functions of CA3; and (b) the loss of DG-specific mnemonic functions, namely ‘pattern separation’, a change that could increase the prevalence of illusory pattern completion and reduce discrimination between present and past experiences in memory. The resulting increase in ‘runaway’ CA3-mediated pattern completion could result in cognitive ‘mistakes’, generating psychotic associations and resulting in memories with psychotic content. Tests of this model could result in novel approaches to the treatment of psychosis and declarative memory alterations, and novel animal preparations for basic schizophrenia research.

At the cellular and molecular levels of operation, neurons and their circuits achieve brain functions by chemical signals, in which the principle agents, neurotransmitters convey the signal from the sending neuron to the receiving neuron. The discovery of each of the chemical families of neurotransmitters ( amino acids, amines and neuropeptides) provide important insights into our understanding of how brains function and the changes in our concepts of the complexities of short term and longer term brain events, and the means by which medications can intervene in brain dysfunctions.

Recent advances in noninvasive neuroimaging have set the stage for the systematic exploration of human brain circuits in health and disease. The Human Connectome Project (HCP) is systematically characterizing brain circuitry, its variability, and its relation to behavior in a population of 1,200 healthy adults (twins and their non-twin siblings). This talk will review progress by the HCP consortium in acquiring, analyzing, and freely sharing these massive and highly informative datasets. The HCP obtains information about structural and functional connectivity using diffusion MRI and resting-state fMRI, respectively. Additional modalities include task-evoked fMRI and MEG, plus extensive behavioral testing and genotyping. Each of these methods is powerful, yet faces significant technical limitations that are important to characterize and be mindful of when interpreting neuroimaging data. Advanced visualization and analysis methods developed by the HCP enable characterization of brain circuits in individuals and group averages at high spatial resolution and at the level of functionally distinct brain parcels and brain networks. Comparisons across subjects are beginning to reveal aspects of brain circuitry that are heritable or are related to particular behavioral capacities. Data from the HCP is being made freely available to the neuroscience community via a user-friendly informatics platform. Altogether, the HCP is providing invaluable information about the healthy human brain and its variability.

This presentation will include both preclinical and small clinical studies with details on mechanism of action, safety and efficacy of a candidate drug that has the capability of alleviating dysregulation of the dopaminergic system and also, although less clearly documented, the serotonergic system, with potential usefulness in a variety of CNS disorders.

Traditional psychiatric textbooks describe schizophrenia as a clinical enigma of unknown aetiology. However, this is no longer true. We now know a great deal about the risk factors, or contributory causes, of schizophrenia. These can be roughly divided into two main types; those which result in a) aberrant neurodevelopment and b) those which cause dopamine dysregulation; both characteristic abnormalities found in schizophrenia.
Genetic factors are, of course, pre-eminent. These will be discussed elsewhere. However, certain environmental factors have been consistently associated with schizophrenia. Some such as adverse obstetric events (e.g. prenatal infection, perinatal hypoxia) impair neurodevelopment. Others such as abuse of drugs such as amphetamines, cocaine and cannabis which increase striatal dopamine also increase risk. In recent years it has become clear that heavy use of high potency cannabis is responsible for a significant proportion of psychosis. Psychotogenic "legal highs" such as synthetic cannabinoids and cathinones are becoming an increasing cause of acute psychosis.
A range of social adversities such as child abuse, adverse life events, migration/minority ethnicity appear also to facilitate dopamine dysregulation and consequent psychosis. Curiously, psychosis is more common in those born and brought up in large cities than in rural areas. Most recently, it has become clear that the incidence is much higher in cities in Northern countries such as UK and Holland than in both rural and urban areas in Spain and Italy. The exact reason(s) for these differences are unclear but speculation centres on social fragmentation and social isolation.
The challenge for researchers is now to trace the pathogenic pathways from risk factors to psychosis.

Impulsivity can be defined as the tendency to act prematurely without foresight. Behavioural and neurobiological analysis of this construct, based on evidence from both animal and human studies, defines several dissociable forms depending on distinct cortico-striatal substrates. One form of impulsivity depends on the temporal discounting of reward, and another on motor or response disinhibition. Impulsivity is commonly associated with addiction to drugs from different pharmacological classes, but its causal role in human addiction is unclear. I will characterize in neurobehavioral and neurochemical terms a rodent model of impulsivity based on premature responding in an attentional setting. Evidence will be surveyed that high impulsivity on this task precedes the escalation subsequently of cocaine self-administration behavior, as well as a tendency toward compulsive cocaine-seeking and to relapse. These results indicate that the vulnerability to stimulant addiction may depend on an impulsivity endophenotype. Implications of these findings for the aetiology, development, and treatment of drug addiction are considered in the light of recent evidence from studies of human chronic stimulant abusers and their non-drug abusing siblings. I will also consider the neuropsychological basis of compulsivity which can be defined as aberrant perseverative behaviour, and for which obsessive-compulsive behaviour (OCD) is probably the prototypical disorder. I will identify (i) distinct cortical-striatal substrates for compulsive responding which reflect the neural bases of goal-directed and habit learning and (ii) candidate neuroendophenotypes for OCD. I will also address the issue of possible commonalities and differences in the compulsivity of chronic substance abuse and OCD.

Since the discovery and maturing of in vitro techniques that characterized neurotransmitter receptor systems in animal and human brain and subsequent development of in vitro and in vivo autoradiography, there was always a clear scientific motivation to carry out these measurements in living brain. In the early 1980s, this was realized by both in vivo preclinical and ultimately human imaging of neurotransmitter (NT) systems starting with dopamine opiate and serotonin system. Now, some 30 years later, the in vivo imaging of (NT) receptor systems, primarily employing the methodology known as positron emission tomography (PET), single photon imaging computer tomography (SPECT) and other chemical measures including magnetic resonance spectroscopy (MRS) and pfMRI (pharmacologic magnetic resonance imaging) have dramatically established these approaches as valuable tools for neuroscience research.

There is growing interest internationally in elucidating the clinical and biological profile of those at high genetic risk to bipolar disorder (BD) so as to enable the development of targeted early intervention programs. This presentation will focus on the emerging findings from our group and others – highlighting both prospective and cross-sectional reports. Clinical studies are now converging in finding increased rates of both anxiety and behavioural disorders in this group, with three sites reporting that these disorders increase the risk of later development of affective disorders. Cross-sectional neuropsychological studies of first degree relatives of those with BD have previously suggested impairments in verbal learning and working memory, but prospective studies such as our own have not confirmed such findings, suggesting that the well-documented impairments in those with established BD may represent sequelae of the illness. Molecular genetic studies from our own work and a UK group have demonstrated an enrichment of BD polygenic risk alleles in young high risk individuals. Neuroimaging studies – both structural and functional – are now indicating differences compared to controls without any family history of mental illness. Our own initial fMRI study reported reduced inferior frontal gyrus (IFG) activation during response inhibition to emotional stimuli, suggesting a potential trait marker of vulnerability to BD. We have subsequently found, using dynamic causal modelling, that this impaired IFG activation appears to be due to a specific network disturbance suggesting dysfunction in the processes that support hierarchical relationships between emotion and cognitive control. Other groups have also reported functional and structural evidence implicating the IFG in those at high risk of BD. Our preliminary functional and structural (DTI) connectivity analyses are also indicating impaired connections between the IFG and other relevant brain regions.

Behaviors are motivated by two emotional valences: Seeking pleasure and avoiding pain. The ability to select appropriate behavioral responses to environmental stimuli, such as avoiding a predator or approaching a food source, is critical for survival. The perturbation of valence processing is also relevant to a number of psychiatric disease states. Within a given type of behavior, such as feeding or social interaction, motivational drives of both positive and negative valence can contribute. For example, feeding can be driven by the rewarding aspects of food consumption or by the motivation to escape the aversive state of hunger. Recent insights from our lab outline a diverse set of circuit-level processes that can modulate valence in a given behavior. We hope these basic science insights will lead to the development of more effective and specific therapeutics capitalizing on a solid understanding of neural circuitry.

DARPA’s investments aim to leverage brain-function research to alleviate the burden of illness and injury and provide novel, neurotechnology-based capabilities for military personnel and civilians alike. In addition, DARPA is working to improve researchers’ ability to understand the brain by fostering advancements in data handling, imaging, and advanced analytics. This presentation will provide insight to the latest developments in DARPA's brain function research in support of the President's BRAIN Initiative.

The NIH BRAIN initiative, informed by the report from the scientific community (BRAIN 2025) is underway. The major funded efforts at this time fit into 3 main categories; 1) defining the components of brain circuits, i.e., a cell census; 2) developing and testing tools for recording high density information on circuit structure, activity, and manipulating circuit activity; 3) novel technology for noninvasive interrogation and manipulation of circuit activity (next generation imaging). The BRAIN oversight committee provides guidance to NIH as we move forward to engage scientists from computation and physical sciences as well as neuroethics in this historic undertaking. BRAIN is poised to develop the neurotechnologies that enable exploration of the neural basis of human behavior as well as the circuit dysfunction that underlies the disability of neuro/mental/substance abuse disorders.

The dopamine-containing neurons of the midbrain have been implicated in a broad array of psychiatric disorders, ranging from schizophrenia to drug abuse and depression. However, studies seem to indicate that it is not the dopamine neurons themselves that are responsible for these pathological states, but instead the disorders appear to arise due to a disruption of dopamine neuron regulation by afferent inputs. Dopamine neurons recorded in vivo are known to exhibit multiple functional activity states, including baseline tonic firing and phasic activation in response to salient stimuli. Phasic burst firing is believed to be the behaviorally relevant “signal” of the dopamine neuron, whereas the level of tonic discharge represents the “gain” or the level of amplification of this signal. This tonic gain is differentially regulated by multiple brain regions, including the hippocampus, the amygdala, and the prefrontal cortex. Disruptions in these regions can interfere with the normal tonic/phasic balance within the dopamine system. Electrophysiological and behavioral studies in animal models of psychiatric disorders, as well as and human imaging studies in patients, suggest that this disruption may underlie the pathological state of the dopamine system that is present in psychiatric disorders. Specifically, we found that hippocampal hyperactivity in schizophrenia may be responsible for the hyperdopaminergic state of psychosis, whereas prefrontal cortical-amygdala overdrive diminishes reward-related dopamine neuron activity leading to anhedonia in depression. This type of information can contribute both to a better understanding of the pathophysiology of major psychiatric disorders, as well as glean insights into novel avenues of treatment and potentially in preventing the emergence of these disorders.

Schizophrenia is a severe psychiatric disorder affecting 1% of the world’s population, leading to high human, social and economic burdens. Understanding how the interaction of gene and environment risk factors during neurodevelopment leads to cognitive, affective and social impairment is a central challenge in schizophrenia pathophysiology. I will discuss how these risk factors converge on a hub composed of NMDA-receptor hypofunction, neuroinflammation and redox imbalance/oxidative stress, leading to structural and functional dysconnectivity. Based on oxidative stress markers and genetic associations in patients, this hypothesis received support from a glutathione deficit preclinical model (gclm -/-mice), reproducing numerous schizophrenia phenotypes including NMDA receptor hypofunction, inflammation, impaired parvalbumine fast-spiking GABA interneurons (PVI), myelination, neural synchronization and behavioral anomalies. This model also highlights childhood and peripuberty as critical periods of high vulnerability for environmental adverse insults. Indeed, additional oxidative challenges in juvenile and peripubertal ages, but not in adult gclm-/- mice, lead to severe and permanent PVI impairment. Regulation of redox state in PVI also balances plasticity and stability across cortical development, through delaying and/or keeping critical periods of plasticity open-ended. Moreover, long range connections may also be affected by redox dysregulation during development: gclm-/- mice present myelin marker deficits in the prefrontal cortex at peripuberty, involving the Fyn kinase pathway dysregulation, which lead to decreased oligodendrocyte proliferation. Most importantly, the antioxidant and GSH precursor N-acetyl-cysteine (NAC), prevents the morphological, biochemical, physiological and behavioral alterations described above. A translational approach towards prevention attempts to modify the disease course by redox modulators will be presented.

The hippocampal formation is one of the most extensively studied regions of the brain, with well described anatomy and basic physiology; moreover, aspects of human memory mediated by hippocampus are well characterized. In schizophrenia, alterations in hippocampal anatomy, perfusion and activation are consistently reported; impairments in declarative memory function, especially in the flexible use of event memories (e.g., in the service of memory-based inference), are common. Postmortem molecular changes suggest a selective reduction in glutamate transmission in the dentate gyrus (DG) and in its efferent fibers, the mossy fiber pathway. A reduction in DG glutamatergic output and in its information processing functions could generate two co-occurring outcomes in hippocampus: (a) a change in homeostatic plasticity processes in CA3, accompanied by increased activity due to reduced afferent stimulation from DG onto CA3 neurons, a process that could increase the ‘pattern completion’ functions of CA3; and (b) the loss of DG-specific mnemonic functions, namely ‘pattern separation’, a change that could increase the prevalence of illusory pattern completion and reduce discrimination between present and past experiences in memory. The resulting increase in ‘runaway’ CA3-mediated pattern completion could result in cognitive ‘mistakes’, generating psychotic associations and resulting in memories with psychotic content. Tests of this model could result in novel approaches to the treatment of psychosis and declarative memory alterations, and novel animal preparations for basic schizophrenia research.

Traditional psychiatric textbooks describe schizophrenia as a clinical enigma of unknown aetiology. However, this is no longer true. We now know a great deal about the risk factors, or contributory causes, of schizophrenia. These can be roughly divided into two main types; those which result in a) aberrant neurodevelopment and b) those which cause dopamine dysregulation; both characteristic abnormalities found in schizophrenia.
Genetic factors are, of course, pre-eminent. These will be discussed elsewhere. However, certain environmental factors have been consistently associated with schizophrenia. Some such as adverse obstetric events (e.g. prenatal infection, perinatal hypoxia) impair neurodevelopment. Others such as abuse of drugs such as amphetamines, cocaine and cannabis which increase striatal dopamine also increase risk. In recent years it has become clear that heavy use of high potency cannabis is responsible for a significant proportion of psychosis. Psychotogenic "legal highs" such as synthetic cannabinoids and cathinones are becoming an increasing cause of acute psychosis.
A range of social adversities such as child abuse, adverse life events, migration/minority ethnicity appear also to facilitate dopamine dysregulation and consequent psychosis. Curiously, psychosis is more common in those born and brought up in large cities than in rural areas. Most recently, it has become clear that the incidence is much higher in cities in Northern countries such as UK and Holland than in both rural and urban areas in Spain and Italy. The exact reason(s) for these differences are unclear but speculation centres on social fragmentation and social isolation.
The challenge for researchers is now to trace the pathogenic pathways from risk factors to psychosis.

There is growing interest internationally in elucidating the clinical and biological profile of those at high genetic risk to bipolar disorder (BD) so as to enable the development of targeted early intervention programs. This presentation will focus on the emerging findings from our group and others – highlighting both prospective and cross-sectional reports. Clinical studies are now converging in finding increased rates of both anxiety and behavioural disorders in this group, with three sites reporting that these disorders increase the risk of later development of affective disorders. Cross-sectional neuropsychological studies of first degree relatives of those with BD have previously suggested impairments in verbal learning and working memory, but prospective studies such as our own have not confirmed such findings, suggesting that the well-documented impairments in those with established BD may represent sequelae of the illness. Molecular genetic studies from our own work and a UK group have demonstrated an enrichment of BD polygenic risk alleles in young high risk individuals. Neuroimaging studies – both structural and functional – are now indicating differences compared to controls without any family history of mental illness. Our own initial fMRI study reported reduced inferior frontal gyrus (IFG) activation during response inhibition to emotional stimuli, suggesting a potential trait marker of vulnerability to BD. We have subsequently found, using dynamic causal modelling, that this impaired IFG activation appears to be due to a specific network disturbance suggesting dysfunction in the processes that support hierarchical relationships between emotion and cognitive control. Other groups have also reported functional and structural evidence implicating the IFG in those at high risk of BD. Our preliminary functional and structural (DTI) connectivity analyses are also indicating impaired connections between the IFG and other relevant brain regions.

The dorsal anterior cingulate cortex (dACC), orbitofrontal cortex (OFC), ventrolateral and ventromedial prefrontal cortex (vlPFC, vmPFC) and their connections with the basal ganglia play a central role in reward and decision-making. These areas, along with their white matter pathways, are closely associated with several psychiatric disorders, including depression, obsessive–compulsive disorder (OCD), and addiction. While their connections define the reward-related cortical and basal ganglia regions, their terminals also interface in specific locations with those from cognitive control cortical areas. These regions, specifically located in the dACC, vlPFC, and striatum, are in pivotal positions for providing a ‘platform’ for bottom-up and/or top down control of goal directed behaviors. The first part of this talk will address the connectivity of the reward circuit and its interface with cognitive control cortical regions. Axons from reward-related and cognitive control cortical areas travel through several white matter bundles, that shows changes in volume and diffusivity in several psychiatric disorders. Importantly, these WM bundles are targets for invasive surgeries for treatment of depression and OCD, including lesions and deep brain stimulation (DBS). For example, anterior capsulotomy and DBS, two surgical treatments for OCD and depression, target the internal capsule. Lesions of the dorsal cingulum bundle (cingulotomy), is also a target for depression and OCD, and the subgenual cingulum bundle is a DBS target for depression. The second part of this talk will demonstrate the PFC fiber positions through these bundles demonstrating the likely connections captured at the three surgical targets.

The Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative has the ambitious goal of elucidating how neuronal ensembles interactively encode higher brain processes. To accomplish this goal, new and improved methods for both recording and manipulating neuronal activity will be needed. In this thal, I will focus on technologies for manipulating neuronal activity. In particular I will present an enhanced chemogenetic toolbox that allows non-invasive, multiplexed spatiotemporal control of neuronal activity in domains ranging from single synapses to ensembles of neurons.

Behaviors are motivated by two emotional valences: Seeking pleasure and avoiding pain. The ability to select appropriate behavioral responses to environmental stimuli, such as avoiding a predator or approaching a food source, is critical for survival. The perturbation of valence processing is also relevant to a number of psychiatric disease states. Within a given type of behavior, such as feeding or social interaction, motivational drives of both positive and negative valence can contribute. For example, feeding can be driven by the rewarding aspects of food consumption or by the motivation to escape the aversive state of hunger. Recent insights from our lab outline a diverse set of circuit-level processes that can modulate valence in a given behavior. We hope these basic science insights will lead to the development of more effective and specific therapeutics capitalizing on a solid understanding of neural circuitry.

At the cellular and molecular levels of operation, neurons and their circuits achieve brain functions by chemical signals, in which the principle agents, neurotransmitters convey the signal from the sending neuron to the receiving neuron. The discovery of each of the chemical families of neurotransmitters ( amino acids, amines and neuropeptides) provide important insights into our understanding of how brains function and the changes in our concepts of the complexities of short term and longer term brain events, and the means by which medications can intervene in brain dysfunctions.

Recent advances in noninvasive neuroimaging have set the stage for the systematic exploration of human brain circuits in health and disease. The Human Connectome Project (HCP) is systematically characterizing brain circuitry, its variability, and its relation to behavior in a population of 1,200 healthy adults (twins and their non-twin siblings). This talk will review progress by the HCP consortium in acquiring, analyzing, and freely sharing these massive and highly informative datasets. The HCP obtains information about structural and functional connectivity using diffusion MRI and resting-state fMRI, respectively. Additional modalities include task-evoked fMRI and MEG, plus extensive behavioral testing and genotyping. Each of these methods is powerful, yet faces significant technical limitations that are important to characterize and be mindful of when interpreting neuroimaging data. Advanced visualization and analysis methods developed by the HCP enable characterization of brain circuits in individuals and group averages at high spatial resolution and at the level of functionally distinct brain parcels and brain networks. Comparisons across subjects are beginning to reveal aspects of brain circuitry that are heritable or are related to particular behavioral capacities. Data from the HCP is being made freely available to the neuroscience community via a user-friendly informatics platform. Altogether, the HCP is providing invaluable information about the healthy human brain and its variability.

This presentation will include both preclinical and small clinical studies with details on mechanism of action, safety and efficacy of a candidate drug that has the capability of alleviating dysregulation of the dopaminergic system and also, although less clearly documented, the serotonergic system, with potential usefulness in a variety of CNS disorders.

Impulsivity can be defined as the tendency to act prematurely without foresight. Behavioural and neurobiological analysis of this construct, based on evidence from both animal and human studies, defines several dissociable forms depending on distinct cortico-striatal substrates. One form of impulsivity depends on the temporal discounting of reward, and another on motor or response disinhibition. Impulsivity is commonly associated with addiction to drugs from different pharmacological classes, but its causal role in human addiction is unclear. I will characterize in neurobehavioral and neurochemical terms a rodent model of impulsivity based on premature responding in an attentional setting. Evidence will be surveyed that high impulsivity on this task precedes the escalation subsequently of cocaine self-administration behavior, as well as a tendency toward compulsive cocaine-seeking and to relapse. These results indicate that the vulnerability to stimulant addiction may depend on an impulsivity endophenotype. Implications of these findings for the aetiology, development, and treatment of drug addiction are considered in the light of recent evidence from studies of human chronic stimulant abusers and their non-drug abusing siblings. I will also consider the neuropsychological basis of compulsivity which can be defined as aberrant perseverative behaviour, and for which obsessive-compulsive behaviour (OCD) is probably the prototypical disorder. I will identify (i) distinct cortical-striatal substrates for compulsive responding which reflect the neural bases of goal-directed and habit learning and (ii) candidate neuroendophenotypes for OCD. I will also address the issue of possible commonalities and differences in the compulsivity of chronic substance abuse and OCD.

Since the discovery and maturing of in vitro techniques that characterized neurotransmitter receptor systems in animal and human brain and subsequent development of in vitro and in vivo autoradiography, there was always a clear scientific motivation to carry out these measurements in living brain. In the early 1980s, this was realized by both in vivo preclinical and ultimately human imaging of neurotransmitter (NT) systems starting with dopamine opiate and serotonin system. Now, some 30 years later, the in vivo imaging of (NT) receptor systems, primarily employing the methodology known as positron emission tomography (PET), single photon imaging computer tomography (SPECT) and other chemical measures including magnetic resonance spectroscopy (MRS) and pfMRI (pharmacologic magnetic resonance imaging) have dramatically established these approaches as valuable tools for neuroscience research.

DARPA’s investments aim to leverage brain-function research to alleviate the burden of illness and injury and provide novel, neurotechnology-based capabilities for military personnel and civilians alike. In addition, DARPA is working to improve researchers’ ability to understand the brain by fostering advancements in data handling, imaging, and advanced analytics. This presentation will provide insight to the latest developments in DARPA's brain function research in support of the President's BRAIN Initiative.

The NIH BRAIN initiative, informed by the report from the scientific community (BRAIN 2025) is underway. The major funded efforts at this time fit into 3 main categories; 1) defining the components of brain circuits, i.e., a cell census; 2) developing and testing tools for recording high density information on circuit structure, activity, and manipulating circuit activity; 3) novel technology for noninvasive interrogation and manipulation of circuit activity (next generation imaging). The BRAIN oversight committee provides guidance to NIH as we move forward to engage scientists from computation and physical sciences as well as neuroethics in this historic undertaking. BRAIN is poised to develop the neurotechnologies that enable exploration of the neural basis of human behavior as well as the circuit dysfunction that underlies the disability of neuro/mental/substance abuse disorders.

BioConference Live makes it easier and more cost-effective for the neuroscience research community to come together online through live video webcasts and real-time networking. BioConference Live attendees learn new concepts, tools and techniques that they can apply to research and diagnosis. BioConference Live requires no travel or time away from the lab or hospital, yet delivers all the benefits of a physical conference. Attendees can earn free CME and CE Credits.

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Floyd E. Bloom, M.D.is professor emeritus at The Scripps Research Institute in La Jolla, California. He was chairman emeritus of the department of neuropharmacology at The Scripps Research Institute, past president of the American Association for the Advancement of Science, former president of the Society for Neuroscience and of the American College of Neuropsychopharmacology, former editor-in-chief of Science (1995-2000), director of behavioral neurobiology at the Salk Institute for Biological Studies, and chief of the Laboratory of Neuropharmacology of the National Institute of Mental Health. Dr. Bloom recently won the RSA Lifetime Achievement Award at the Research Society on Alcoholisms annual meeting in June 2012 in San Francisco, California.

Anthony Grace, PhD

Distinguished Professor of Neuroscience, Professor of Psychiatry and Psychology Department of Neuroscience, University of Pittsburgh

Dr. Anthony A. Grace is a Distinguished Professor of Neuroscience and a Professor of Psychiatry and Psychology at the University of Pittsburgh in Pittsburgh, PA.&nbsp; He received his Ph.D. from Yale University School of Medicine with Dr. Benjamin S. Bunney and had postdoctoral training with Dr. Rodolfo Llinas in the Department of Physiology and Biophysics at New York University School of Medicine.&nbsp; Dr. Grace has been involved in translational research related to the dopamine system for over 30 years.&nbsp;&nbsp; His early work pioneered the mode of action of antipsychotic drugs, and the identification and characterization of dopamine-containing neurons, and was the first to provide a means to quantify their activity state and pattern in a way that is the standard in the literature.&nbsp; His current work involves novel treatments for schizophrenia and its prevention, the role of dopamine in anhedonia and affective disorders, and the mode of action of ketamine and novel antidepressant drugs.&nbsp; Dr. Grace has received several awards for his research, including the Paul Janssen Schizophrenia Research Award and the Lilly Basic Scientist Award from the International College of Neuropsychopharmacology, the Efron Award from the American College of Neuropsychopharmacology, as well as a NIMH MERIT award, a Distinguished Investigator award from the National Alliance for Research in Schizophrenia and Depression, the Judith Silver Memorial Investigator Award from the National Alliance for the Mentally Ill, a Fellow of the American Association for the Advancement of Science, and appointment as a Distinguished Professor of Neuroscience at the University of Pittsburgh.&nbsp; He is also a past member of the governing council of the American College of Neuropsychopharmacology and is on the editorial board fornumerous leading journals in the field.
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Arvid Carlsson, Swedish pharmacologist who, along with Paul Greengard and Eric Kandel, was awarded the 2000 Nobel Prize for Physiology or Medicine for his research establishing dopamine as an important neurotransmitter in the brain.
Carlsson received a medical degree from the University of Lund in 1951 and subsequently held teaching positions there until 1959, when he became professor of pharmacology at the University of Gothenburg. When Carlsson began his pioneering studies in the 1950s, scientists thought that dopamine worked only indirectly, by causing brain cells to make another neurotransmitter, noradrenaline. Using a sensitive test that he had devised, Carlsson detected particularly high levels of the compound in areas of the brain that controlled walking and other voluntary movements. In animal experiments he showed that depletion of dopamine impairs the ability to move. When Carlsson treated dopamine-depleted animals with the amino acid l-dopa, the symptoms disappeared, and the animals moved normally again. This led to the use of l-dopa as a treatment for Parkinson disease, and it eventually became the single most important medication for the disease. Carlsson's work also contributed to an understanding of the relationship between neurotransmitters and mental states and led to the introduction of new antidepressant drugs.

Trevor Robbins, CBE FRS FMedSci FBPsS

Head of Department of Psychology, Professor of Cognitive Neuroscience, University of Cambridge

Trevor Robbins was appointed in 1997 as the Professor of Cognitive Neuroscience at the University of Cambridge. He was elected to the Chair of Experimental Psychology (and Head of Department) at Cambridge from October 2002. He is also Director of the Behavioural and Clinical Neuroscience Institute (BCNI), jointly funded by the Medical Research Council and the Wellcome Trust. The mission of the BCNI is to inter-relate basic and clinical research in psychiatry and neurology for such conditions as Parkinson's, Huntington's, and Alzheimer's diseases, frontal lobe injury, schizophrenia, depression, drug addiction and developmental syndromes such as attention deficit/hyperactivity disorder.
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<br />Trevor is a Fellow of the British Psychological Society (1990), the Academy of Medical Sciences (2000) and the Royal Society (2005). In 2014 he was awarded a share of the Grete Lundbeck Brain Prize. He was also given the American Psychological Association's Distinguished contribution award in 2011. He has been President of the European Behavioural Pharmacology Society (1992-1994) and he won that Society's inaugural Distinguished Scientist Award in 2001. He was also President of the British Association of Psychopharmacology from 1996 to 1997. He has edited the journal Psychopharmacology since 1980 and joined the editorial board of Science in January 2003. He has been a member of the Medical Research Council (UK) and chaired the Neuroscience and Mental Health Board from 1995 until 1999.
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<br />He has been included on a list of the 100 most cited neuroscientists by ISI, has published over 600 full papers in scientific journals and has co-edited seven books (Psychology for Medicine: The Prefrontal Cortex; Executive and Cognitive Function: Disorders of Brain and Mind 2:Drugs and the Future: The Neurobiology of Addiction; New Vistas. Decision-making, Affect and Learning: and, Cognitive Search: Evolution, Algorithms, and the Brain).
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Dr. Tamminga holds the Lou and Ellen McGinley Distinguished Chair and the McKenzie Chair in Psychiatry at the University of Texas Southwestern Medical School and is the Chairman of the Department of Psychiatry and the Chief of the Translational Neuroscience Division in Schizophrenia at UTSW.&nbsp;&nbsp; She received her M.D. degree from Vanderbilt University and completed residency training in psychiatry at the University of Chicago.&nbsp; She served on the University of Chicago faculty from 1975 to 1979 and moved to the NINDS for training in Neurology in 1978.&nbsp;&nbsp; After joining the faculty at the University of Maryland Medical School in 1979, she practiced research, clinical care and teaching there until joining the faculty at UT Southwestern Medical School in 2003.
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<br />Dr. Tamminga is currently a member of NIMHs National Advisory Board and has served on the Board of Scientific Counselors of the National Institute of Mental Health and the National Institute of Drug Abuse, as Council member and President of the American College of Neuropsychopharmacology, as a Member and Chair of the Psychopharmacological Drugs Advisory Committee of the FDA, as well as consultant for the Orphan Products Development Review Group, FDA.&nbsp; She is a member of the Advisory Board of the Brain and Behavioral Research Foundation (NARSAD).&nbsp;&nbsp; She is currently the Deputy Editor of the American Journal of Psychiatry and on the editorial board of several other journals in the field.&nbsp;&nbsp; Dr. Tamminga was elected to the Institute of Medicine of the National Academies of Sciences in 1998 and has served on several IOM committees in that capacity.
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Sir Robin Murray, PhD

Professor of Psychiatric Research, Institute of Psychiatry, King's College London

Robin Murray is Professor of Psychiatric Research at the Institute of Psychiatry, and indeed has spent most of his working life there apart from one year in the USA: fortunately the latter did not do him too much harm. His particular interest is in understanding the causes of psychosis, and he and his colleagues have contributed to the understanding that environmental factors such as obstetric events, heavy cannabis use and migration increase the risk of developing schizophrenia-like psychoses. He is also sees people with psychosis at the South London and Maudsley NHS Trust who are been referred from across the UK because they have not responded to treatment locally. He has written numerous articles, not all of the boring, and is the second most frequently cited psychiatrist outside the USA; he has supervised 52 PhDs and 35 of his students have become professors. He was elected a Fellow of the Royal Society in 2010 and received a knighthood in 2011.

Philip Mitchell AM, MB BS (Hons I), MD, FRANZCP, FRCPsych

Scientia Professor and Head of the School of Psychiatry, University of New South Wales

Philip Mitchell is Scientia Professor and Head of the School of Psychiatry at University of New South Wales in Sydney, Australia; Member, Australian National Health and Medical Research Council Research Committee; Vice-President (Governance), International Society for Bipolar Disorders; and Board Member, Black Dog Institute.
His research and clinical interests are in bipolar disorder and depression, with a particular focus on: predictors of the development of bipolar disorder in at-risk individuals; molecular genetics of bipolar disorder; pharmacological and psychological treatments for bipolar disorder and depression; clinical phenomenology of bipolar disorder and depression; and neurostimulatory therapies for depression. Professor Mitchell has published over 450 peer-reviewed papers or book chapters and is lead investigator on an Australian NHMRC-funded Program Grant on depression and bipolar disorder. He serves on the editorial boards of ‘Psychiatric Genetics', ‘CNS Drugs', ‘CNS Spectrums', ‘Frontiers in Behavioral and Psychiatric Genetics', ‘Future Neurology', ‘International Journal of Bipolar Disorders', ‘Medicine Today' and ‘Therapeutic Advances in Psychopharmacology'.
In 2002 he was awarded the Senior Research Award of the Royal Australian and New Zealand College of Psychiatrists (RANZCP). In 2004, he received the Founders Medal of the Australasian Society for Psychiatry Research. In 2008, he was invited to give the endowed Samuel Novey Lecture in Psychological Medicine at Johns Hopkins University, Department of Psychiatry and Behavioral Sciences. In the 2010 Australia Day honours list Professor Mitchell was appointed as a Member of the Order of Australia for service to medical education, particularly in the field of psychiatry, as an academic, researcher and practitioner, through contributions to the understanding, treatment and prevention of mental illnesses. In 2013 he was awarded the College Citation of the RANZCP for exceptional service to psychiatry.

Dean Wong, MD, PhD

Radiology Vice Chair for Research Administration and Training, Professor of Radiology and Radiological Science, Johns Hopkins University School of Medicine

Dr. Dean Foster Wong is a Professor in the Johns Hopkins Medicine Department of Radiology and Radiological Science. He also serves as Radiology Vice Chair for Research Administration and Training, and Director of the Section of High Resolution Brain PET Imaging within the Division of Nuclear Medicine.
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<br />Dr. Wong received his undergraduate degree in physics from the University of Western Ontario, and completed his M.D. at the University of Toronto in 1977. After an internship at Sunnybrook Medical Center in Toronto, he undertook a residency in anatomic pathology at Princess Margaret Hospital of the Ontario Cancer Institute, and a subsequent residency in radiology at the University of Toronto.
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<br />In 1980, he came to Johns Hopkins as a research and clinical fellow in the Radiology Division of Nuclear Medicine. He was soon promoted to Assistant Professor of Radiology, and in 1987 became an Associate Professor. He received a doctorate in Radiation Health Sciences from Hopkins in 1990.
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<br />Over the course of his career, Dr. Wong has been a leader in the design, development and use of PET scanning for the study of brain chemistry. He has been primary investigator on numerous federal and private grants, has authored or coauthored more than 200 articles and 50 book chapters and essays, and has been an active consultant to pharmaceutical companies.
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<br />In 2013, the Society of Nuclear Medicine and Molecular Imaging bestowed upon him the Paul C. Aebersold Award for Outstanding Achievement in Basic Nuclear Medicine Science.
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Suzanne Haber, PhD

Professor, Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry

Dr. Habers research focuses on the neural network underlying learning and decision-making that leads to action plan development. The cortico-basal ganglia-thalamic system is central to this network and comprises a diverse group of structures involved in reward and motivation, cognition and motor control. Pathology of this network is implicated in several mental health disorders including drug addiction, obsessive-compulsive disorder, and schizophrenia. Her lab is addressing the hypothesis that cortico-basal ganglia connections are critical for integrating information across functional domains. The lab is also investigating which pathways are stimulated during deep brain stimulation, a therapy now being actively investigated for depression and obsessive-compulsive disorder and understanding postnatal changes in the cortico-basal ganglia system associated with specific developmental milestones and the high level of plasticity during early learning.
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<br />Dr. Haber received her Ph.D. in neuro-and bio-behavioral sciences from Stanford University.
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Bryan L. Roth MD, PhD is the Michael Hooker Distinguished Professor of Protein Therapeutics and Translational Proteomics in the Department of Pharmacology at the University of North Carolina at Chapel Hill Medical School.&nbsp; Dr. Roth has published more than 300 papers and has given more than 200 invited talks. Dr. Roth has served on the editorial boards of many major scientific journals including the Journal of Biological Chemistry, Molecular Pharmacology, the Journal of Pharmacology and Experimental Therapeutics, ACS Medicinal Chemistry Letters, The Journal of Receptors and Signal Transduction Research, the Journal of Neurochemistry, Pharmacology and Therapeutics, Psychopharmacology and Neuropsychopharmacology.&nbsp; Dr Roth is currently Associate Editor for the Journal of Clinical Investiagation.&nbsp;&nbsp; Dr. Roth is also a member of Faculty of 1000.
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<br />Dr. Roth has received a number of honors including the PhRMA Foundation Excellence in Pharmacology Award, the Irving Page Lecture, the NARSAD Distinguished Investigator Award, the Heffter Foundation Award for Basic Science Research, the Lowenthal Lecture (Medical College of Virginia), a Prestige Lecture (Universit de Montral), the SG Fergusson Memorial Lecture (Robarts Institute), the Chauncy Leake Memorial Lecture (Univ Texas Medical Branch), the National Institute of Mental Health Career Development Award,&nbsp; a Dana Foundation Fellowship in Neurosciences (Stanford University) and Phi Beta Kappa (St. Louis University).&nbsp; Dr. Roths work has been highlighted and Dr. Roth has been interviewed about his work in the New York Times, the Wall Street Journal, National Public Radios All Things Considered, CBS Early Program, MSNBC, the Los Angeles Times and a large number of other media outlets. Dr. Roth was elected to the Institute of Medicine in 2014.
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David Van Essen, PhD

Professor of Anatomy and Neurobiology, Washington University School of Medicine

Dr. Van Essen is currently Edison Professor and Head of the Anatomy & Neurobiology Department at Washington University in St. Louis. He has served as Editor-in-Chief of the Journal of Neuroscience, founding chair of the Organization for Human Brain Mapping, and President of the Society for Neuroscience. He is a fellow of the AAAS and has received the Peter Raven Lifetime Achievement Award from the St. Louis Academy of Science and the Krieg Cortical Discoverer Award from the Cajal Club. Dr. Van Essen received his undergraduate degree in Chemistry in 1967 from Caltech and his graduate degree in neurobiology in 1971 from Harvard. He was a postdoctoral fellow at Harvard under Drs. David Hubel and Torsten Wiesel and did additional postdoctoral work in Norway and England before returning to Caltech in 1976. He was a faculty member in the Division of Biology at Caltech until 1992, during which time he served as Executive Officer for Neurobiology (1982-1989) and Option Representative for the Computation and Neural Systems program (1986-1991). In 1992 he became Edison Professor of Neurobiology and Head of the Department of Anatomy and Neurobiology at Washington University School of Medicine. Dr. Van Essen is internationally known for his research on how the brain organizes and processes visual information. He has made extensive contributions to the understanding of how the brain perceives shape, motion and color and how attention affects neural activity. His work has helped to demonstrate that the brain contains dozens of different areas involved in vision and that these areas are interconnected by hundreds of distinct neural pathways. He and his colleagues have developed powerful new techniques in computerized brain mapping to analyze these visual areas in humans as well as nonhuman primates. This work includes the continued development of an integrated suite of software tools for surface-based analyses of cerebral cortex. These methods are applied to the analysis of cortical structure and function in humans, monkeys and rodents. A broad objective is to develop probabilistic surface-based atlases that accurately convey commonalities as well as differences between individuals.

Following a career in basic research in chemistry, molecular biology and neurobiology (glutatmate and nitric oxide transmission, neuro Research Institute (Zurich University), I moved towards "bench to bed" research at the Center for Psychiatric Neuroscience (Department of Psychiatry, Lausanne University Hospital). I set up a translational research program aimed at a better understanding of the causes and mechanisms leading to schizophrenia phenotypes in order to develop markers for early diagnosis, new drug targets as well as preventive and therapeutic measures. Building on an innovative hypothesis, I could demonstrate that oxidative stress/redox dysregulation induced, among others, by glutathione (GSH) deficit, may represent a "hub" on which both genetic and environmental risk factors converge during neurodevelopment, leading to the impairment of neural connectivity and synchronization, and to cognitive deficits as observed in patients. These mechanisms have been comprehensively documented in experimental models. Based on these relevant neurobiological data, a precursor of GSH, N administered to chronic patients. This double blind, placebo controlled add trial with NAC showed a net improvement potentials (mismatch negativity), neural synchronization, and produced no side effects. These promising results led a new clinical trial with young patients during their first psychotic episode, paving the way for risk subjects. In addition to my research activities, I serve as director of the Unit of Research in Schizophrenia and director of the Center for Psychiatric Neuroscience, where we also work on professional education and cure of major psychiatric disorders.

Dr. Koroshetz was named Acting Director of NINDS in October, 2014.&nbsp; Prior to this appointment, he served as Deputy Director of NINDS since January, 2007, where he worked with the NINDS Director in program planning and budgeting, and overseeing Institute scientific and administrative functions.
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<br />Before joining NINDS, Dr. Koroshetz served as vice chair of the neurology service and director of stroke and neurointensive care services at Massachusetts General Hospital (MGH). He was also a professor of neurology at Harvard Medical School and has led neurology resident training at MGH since 1990.
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<br />A native of Brooklyn, New York, Dr. Koroshetz graduated from Georgetown University and received his medical degree from the University of Chicago. He trained in internal medicine at the University of Chicago and Massachusetts General Hospital. Dr. Koroshetz trained in neurology at MGH, after which he did post-doctoral studies in cellular neurophysiology at MGH and the Harvard neurobiology department. He joined the neurology staff, first in the Huntingtons Disease unit and then in the stroke and neurointensive care service.
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<br />As a member of the NINDS intramural review and oversight committees, Dr. Koroshetz has been involved in various NINDS symposia and clinical trials, and served as the Institutes representative to the American Neurological Associations Career Development Symposium. He was a member of the NINDS-chaired Brain Attack Coalition (BAC), a group of professional, voluntary and governmental entities dedicated to reducing the occurrence, disabilities, and death associated with stroke.
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Dr. Justin Sanchez joined DSO as a program manager in 2013. At DARPA, Dr. Sanchez will explore neurotechnology, brain science and systems neurobiology.
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<br />Before coming to DARPA, Dr. Sanchez was an Associate Professor of Biomedical Engineering and Neuroscience at the University of Miami, and a faculty member of the Miami Project to Cure Paralysis. He directed the Neuroprosthetics Research Group, where he oversaw development of neural-interface medical treatments and neurotechnology for treating paralysis and stroke, and for deep brain stimulation for movement disorders, Tourettes syndrome and Obsessive-Compulsive Disorder.
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<br />Dr. Sanchez has developed new methods for signal analysis and processing techniques for studying the unknown aspects of neural coding and functional neurophysiology. His experience covers in vivo electrophysiology for brain-machine interface design in animals and humans where he studied the activity of single neurons, local field potentials and electrocorticogram in the cerebral cortex and from deep brain structures of the motor and limbic system.
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<br />He has published more than 75 peer-reviewed papers, holds seven patents in neuroprosthetic design and authored a book on the design of brain-machine interfaces. He has served as a reviewer for the NIH Neurotechnology Study Section, DoDs Spinal Cord Injury Research Program and the Wellcome Trust, and as an associate editor of multiple journals of biomedical engineering and neurophysiology.
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<br />Dr. Sanchez holds Doctor of Philosophy and Master of Engineering degrees in Biomedical Engineering, and a Bachelor of Science degree in Engineering Science, all from the University of Florida.
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Kay Tye began her education as an undergraduate research assistant at MIT from 1999-2003. She continued her studies at the University of California, San Francisco as a graduate student in Patricia Janaks lab studying electrophysiological properties of amygdala neurons both in vivo and ex vivo during reward-seeking behavior. Kay then did a short postdoc with Antonello Bonci, now the intramural director of NIDA, to study synaptic strength following reward learning, followed by a postdoc at Stanford University with Karl Deisseroth where she used novel optogenetic techniques to dissect the neural circuitry underlying psychiatric disease. Kay is currently an Assistant Professor at Massachusetts Institute of Technology in the Picower Institute for Learning and Memory, a member of the Department of Brain and Cognitive Sciences. She is also a NYSCF Neuroscience Robertson Investigator
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Successful Senior Scientific Business Executive with demonstrated expertise growing markets, revenues, product pipelines and expanding technical organizations into new business opportunities. Educational and business management experience in global markets, with quantified
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success in moving technical businesses into new international arenas. Multi-lingual fluency enables in depth penetration into new organizations relating with all levels of employees. Author of numerous peer-reviewed articles, and holder of several patents.

Jimmy Lin, MD, PhD, MHS, is a 2012 TED Fellow and Founder & President of Rare Genomics Institute, the world's first platform to enable any community to leverage cutting-edge biotechnology to advance understanding of any rare disease. Partnering with 18 of the top medical
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institutions, such as Harvard, Yale, Johns Hopkins, and Stanford, RGI helps custom design personalized research projects for diseases so rare that no organization exists to help. Dr. Lin is also a medical school faculty member at the Washington University in St. Louis and led the computational analysis of the first ever exome sequenching studies for any human disease at Johns Hopkins. He has numerous publications in Science, Nature, Cell, Nature Genetics, and Nature Biotechnology, and has been featured in Forbes, Bloomberg, Wall Street Journal, Washington Post, and the Huffington Post.

Agnieszka is currently a Staff Scientist and Laboratory Manager at TessArae, LLC in Sterling, VA, USA. She obtained her PhD at the University of Queensland in Australia in a field of biochemistry, and subsequently worked as a post-doctoral fellow at Queen's University of Belfast
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University of Queensland and Institute for Molecular Biosciences. Since 2005 until 2008 she held a continuing appointment as a lecturer in a School of Dentistry at the University of Queensland and established her own laboratory in area of functional genomics and metabonomics. She has over 10 years of experience in molecular biology, genetics, genomics, biochemistry, microbiology and metabonomics. In addition she has experience as a science writer. Recently Agnieszka served on the Council of the Australian Society for Biochemistry and Molecular Biology and is still active in the society. Currently she is working on novel diagnostic assays for infectious diseases using microarray re-sequencing technology.

The discovery of proteinaceous disease biomarkers and their clinical validation is critically important for the enablement of molecular diagnostics and ultimately, precision medicine. In spite of the importance of biomarkers, research done in the last two decades has yielded
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limited success in enhancing the repertoire of protein biomarkers of disease. This apparent dichotomy is in large part due to the fact that the process from discovery to validation is complex and involves a multidisciplinary collaboration across clinical, biochemical and biophysical disciplines and that that many initiatives sought to identify unique markers for a given disease with perfect correlation. Recent advances in better biomarker discovery strategies, clinical sampling and sample storage, better sample preparation methods that consider the inherent instabilities associated with clinical specimens, better discovery methods and analytical instrumentation suited for assay validation and clinical assays together promise to generate better panel tests for disease biomarkers of clinical significance.
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Dr. Latterich has nearly 20 years of academic and commercial and leadership experience and features an accomplished research career focused on the proteomics-based discovery of novel biomarkers in oncology, respiratory disease and neurodegenerative disorders. Martin is currently CSO at BioScale, a Lexington, MA, based biotechnology corporation commercializing a novel acoustic biomarker quantification platform. Most recently Martin served as a Professor at the Proteogenomics Research Institute for Systems Medicine in San Diego, where his laboratory used proteomics and genomics to discover novel biomarkers of cancer and degenerative disease though a systems biology approach that includes proteomics. He is also the CSO, co-founder and a board member for the non-profit Nicholas Conor Institute for Pediatric Cancer Research. Martin's work at the institute included designing new technologies to enable the better treatment of children with cancer, using personalized medicine technology to match their unique genetic make-up and tumor physiology to available treatment options. He previously served on the faculty of the University of Montreal, McGill University and the Salk Institute. His grant-funded work has been recognized by the 2003 Tier I Canada Research Chair, the 1998 Pew Scholar Award and the 1997 Basil O'Connor Starter Scholar Award. Dr. Latterich also held senior management positions at several biotechnology companies, including Diversa and Illumina, where he headed the proteomics initiatives. He has made significant contributions to the field of cell biology, clinical biomarker discovery, proteomics and genomics. Among his recent discoveries are biomarkers for cancer, respiratory disease and neurodegenerative disorders. Dr Latterich has edited one book on RNAi, is author on over 34 publications in leading scientific journals and is listed on numerous patent applications. Martin is Editor-in-Chief of the scientific journal Proteome Science. He has served on several national and international study sections. He was a postdoctoral fellow in molecular and cell biology in the laboratory of Dr. Randy Schekman at the HHMI and University of California, Berkeley. Dr. Latterich earned his Ph.D. in cell biology and a B.Sc. in biochemistry and molecular biology from Durham University, U.K.

Dr. Johnson-Davis is a medical director of the Clinical Toxicology laboratory, Antifungal Testing and Immunosuppressants Testing at ARUP. Dr. Johnson-Davis received her PhD in pharmacology at the University of Utah and is board certified in clinical chemistry by the American
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Board of Clinical Chemistry. She completed her postdoctoral fellowship in clinical chemistry at the University of Utah, Department of Pathology, and was a postdoctoral research associate at the Center of Human Toxicology at the University of Utah. Dr. Johnson-Davis is a member of various professional societies, including the Academy of Clinical Laboratory Physicians and Scientists and the American Association for Clinical Chemistry.

Bruce W. Hollis, Ph.D. received his B.Sc. and M.Sc. from the Ohio State University and subsequently his Ph.D. from the University of Guelph in 1979. Dr. Hollis then completed an Endocrine Fellowship at The Case Western Reserve University School of Medicine in 1982. Dr. Hollis
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was then Appointed Assistant Professor of Nutrition at Case Western and remained there until 1986 when he moved to The Medical University of South Carolina where to he is Professor of Pediatrics, Biochemistry and Molecular Biology. He is also Director of Pediatric Nutritional Sciences. Dr. Hollis has studied vitamin D metabolism and nutrition for the past 35 years and has been an NIH grant recipient for the past 30 years. His current work focuses on the vitamin D requirements during pregnancy and lactation. Dr. Hollis has in excess of 200 peer reviewed articles in this area of investigation.

Michael F. Holick, Ph.D., M.D. is Professor of Medicine, Physiology and Biophysics; Director of the General Clinical Research Unit; and Director of the Bone Health Care Clinic and the Director of the Vitamin D, Skin and Bone Research Laboratory at Boston University Medical
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Center.
Dr. Holick has made numerous contributions to the field of the biochemistry, physiology, metabolism, and photobiology of vitamin D for human nutrition. Dr. Holick has established global recommendations advising sunlight exposure as an integral source of vitamin D. He has helped increase awareness in the pediatric and medical communities regarding vitamin D deficiency pandemic, and its role in causing not only metabolic bone disease, and osteoporosis in adults, but increasing risk of children and adults developing common deadly cancers, schizophrenia, infectious diseases including TB and influenza, autoimmune diseases including type 1 diabetes and multiple sclerosis, type 2 diabetes, stroke and heart disease. He also observed the pregnant women who were vitamin D deficient were at increased risk for preeclampsia and requiring a C-section. He has written more than 300 pier reviewed articles, edited or wrote 12 books including The Vitamin D Solution and is the recipient of numerous awards including the Linus Pauling Prize in Human Nutrition.

Mark Marzinke, PhD, DABCC earned a Ph.D. in Biochemistry from the University of Wisconsin-Madison and subsequently completed a clinical chemistry fellowship at The Johns Hopkins University in 2012. During his clinical fellowship, Dr. Marzinke focused on the development and
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validation of qualitative and quantitative mass spectrometric assays for the clinical monitoring and quantitation of pain management drugs and anti-neoplastic agents, respectively. Further, he performed large scale proteomics studies aimed at the temporal identification of biomarkers expressed during ovarian cancer progression. Dr. Marzinke is currently an Instructor in the Departments of Pathology and Medicine at the Johns Hopkins University School of Medicine (JHUSOM). He serves as the Director of Preanalytics and General Chemistry in the Core Laboratory of the Johns Hopkins Hospital, where he focuses on workflow analysis and test utilization. Additionally, he is the Associate Director of the Clinical Pharmacology Analytical Lab (CPAL) at the JHUSOM, where he focuses on the development and validation of quantitative mass spectrometric methods in rare matrices to support large clinical trials. His research interests include the development, validation and implementation of assays focused on personalized medicine, including therapeutic drug monitoring and pharmacogenetic testing. Dr. Marzinke is board certified by the American Board of Clinical Chemistry.

Dr. Mauro is an Associate Professor in the Department of Neurobiology at the Scripps Research Institute in La Jolla, California. He is also a co-founder and lead scientist of Promosome, a biotechnology company focused on bioproduction enablement and DNA vaccines. In addition, Dr
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Mauro is a Senior Fellow in Experimental Neurobiology at the Neurosciences Institute in San Diego, California.
Prior to moving to The Scripps Research Institute, Dr. Mauro received his Ph.D. at McGill University in Montreal, Quebec, and continued his studies as a postdoctoral fellow at The Rockefeller University in New York City.
Dr. Mauro studies both fundamental and applied aspects of translational control mechanisms. His basic research is focused on understanding how eukaryotic mRNAs recruit ribosomes, how ribosomes subsequently locate initiation codons, and how ribosomes regulate the translation of specific subsets of mRNAs. Dr. Mauro's applied studies build on his basic research. These applied studies have led to the identification of Translational Enhancer Elements (TEEs) and the generation of synthetic translational enhancers.

Ross J. Molinaro, PhD, MT(ASCP), DABCC, FACB is an Assistant Professor in the Department of Pathology and Laboratory Medicine at Emory University. He received his PhD in Clinical Chemistry and Molecular Medicine from Cleveland State University and completed the ComACC training
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program at Emory as the first recipient of the AACC Past-Presidents' Scholarship. He currently serves as the Medical Director of the Core Laboratory at Emory University Hospital Midtown and co-Director of the Emory Clinical Translational Research Laboratory. Ross also teaches various aspects of laboratory medicine to medical students, pathology residents and fellows, clinical chemistry fellows, and medical technology students.
Ross joined the AACC in 2005 and is a member of the Proteomics and Clinical Translational Science Divisions. Ross is currently a committee member of the Society for Young Clinical Laboratorians (SYCL). He is also a member of the Professional Practice Review Course Curriculum Organizing Committee and the Clinical Chemistry Trainee Council Executive Committee as the Exam Questions Vault Coordinator. In addition, Ross serves as an American Society for Clinical Pathology (ASCP) Board Liaison to the Clinical Chemistry Examination Committee, and a member of the Board of Governors as the ASCP/AACC Member Representative. With over 40 publications and book chapters, his interests reside in the practice and standardization of mass
spectrometry in the clinical laboratory and expanding the knowledge base of clinical chemistry and laboratory medicine for medical students and those practicing in different healthcare disciplines.

Dr. Sihe Wang is Section Head and Medical Director of Clinical Biochemistry and Director of Clinical Biochemistry Fellowship Training Program, Cleveland Clinic, Cleveland, Ohio. He also chairs the clinical chemistry integration effort for the Cleveland Clinic Health System which
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includes 1 Florida hospital, 8 community hospitals and 18 family health centers in Northeast Ohio. Additionally, he is Clinical Chemistry Professor, Cleveland State University. Prior to his current position, Dr. Wang was Assistant Professor at Northwestern University; Director, Clinical Chemistry Laboratory and Referred Testing Laboratory, Children's Memorial Hospital, Chicago, Illinois. Dr. Wang is a diplomate of the American Board of Clinical Chemistry (DABCC) and a fellow of the National Academy of Clinical Biochemistry (FACB).
Dr. Wang is a member of several professional organizations, including the American Society for Mass Spectrometry and the American Association for Clinical Chemistry (AACC). He served as chair of AACC Northeast Ohio Section in 2008 and 2009 and the president of North American Chinese Clinical Chemistry Association (NACCCA) 2008-2009. Currently he serves as the historian for NACCCA, the treasurer for the Pediatric and Maternal Fetal Division of AACC, the delegate for AACC Northeast Ohio section, commissioner for The Commission on Accreditation in Clinical Chemistry (ComACC), and a member of AACC's Strategies Online Editorial Advisory Board. The AACC presented him with the 2005, 2008, and 2010 Clinical Chemist Recognition Award. He is also the recipient of the 2006 Lemuel J. Bowie Young Investigator Award for the Chicago Section of the AACC. Dr. Wang has authored over 140 journal articles, book chapters, and abstracts. He also serves on several editorial boards of peer reviewed journals.

Dr. Taylors background is in biophysics, bioinformatics, computational biology and structural biology with emphasis on human genetics and translational medicine. She obtained her Ph.D. in Biophysics from the University of Michigan, Ann Arbor, and completed a postdoctoral
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fellowship at Pfizer in Ann Arbor. She had worked in the pharmaceutical industry at EMD-Serono, transitioning into clinical and basic research by moving to Harvard School of Public Health and then to clinical research at RWJ/Rutgers. She also served several years as the Program Director of the Graduate Program in Bioinformatics at Brandeis University, where she still occasionally teaches a course in Computational Systems Biology.
Her main areas of research are in the development of mathematical and computational methods to better understand biological variation and the genetic contribution to disease, coupling clinical information with high-dimensional biomedical data from next-gen sequencing, microarray, PCR, and proteomics experiments. Some of her immediate research interests are in development of methods to better classify effects of genetic variation within interacting systems through effects in gene function and contributions to disease, developing mathematical genotype representations of variation in populations, and using machine-learning techniques to build classifiers in translational medicine research. Her scientific contributions were acknowledged with the rest of the Divisions research team at the 2010 ASRM meeting when the REI division received the ASRM Prize Paper Award, where her contribution was in building databases, systems and validated methods for high-throughput genotype analyses .

Dr. Straseski is a medical director of endocrinology at ARUP Laboratories and an assistant professor of pathology at the University of Utah School of Medicine. She received her PhD in pathology and laboratory medicine and a Master's degree in bacteriology from the University of
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Wisconsin-Madison, where she also served as a postdoctoral associate in the Department of Pathology. Dr. Straseski completed a postdoctoral fellowship in clinical chemistry at the Johns Hopkins Medical Institutions in Baltimore, Maryland. She has previously been awarded the Past-President Scholarship by the American Association for Clinical Chemistry, as well as a Distinguished Abstract Award from the National Academy of Clinical Biochemistry. Dr. Straseski is board certified in clinical chemistry by the American Board of Clinical Chemistry.

John Quackenbush received his PhD in 1990 in theoretical physics from UCLA working on string theory models. Following two years as a postdoctoral fellow in physics, Dr. Quackenbush applied for and received a Special Emphasis Research Career Award from the National Center for
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Human Genome Research to work on the Human Genome Project. He spent two years at the Salk Institute and two years at Stanford University working at the interface of genomics and computational biology. In 1997 he joined the faculty of The Institute for Genomic Research (TIGR) where his focus began to shift to understanding what was encoded within the human genome. Since joining the faculties of the Dana-Farber Cancer Institute and the Harvard School of Public Health in 2005, his work has focused on the use of genomic data to reconstruct the networks of genes that drive the development of diseases such as cancer and emphysema.

Judd W. Moul is James H. Semans, MD Professor of Surgery, Division of Urologic Surgery, and Director of the Duke Prostate Center, Duke Cancer Institute at Duke University Medical Center. Prior to joining Duke, he was Professor of Surgery at the Uniformed Services University of
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the Health Sciences (USUHS) in Bethesda, Maryland and an attending Urologic Oncologist at the Walter Reed Army Medical Center (WRAMC) in Washington, DC. In addition, he was Director of the Center for Prostate Disease Research (CPDR); a Congress-mandated research program of the Department of Defense based at USUHS and WRAMC. In 2004, he completed a 26-year U.S. Army career, retiring as a full Colonel in the Medical Corps, and became Chief of the Division of Urologic Surgery at Duke. Serving as Chief from 2004 to 2011, he brought innovation and growth to the program. Most notably, he started the Duke Prostate Center, expanded the urology residency training program through a novel collaboration with the Department of Defense and was able to maintain Duke Urology as a top 10 program in the nation throughout his tenure. Dr Moul completed his Urologic Oncology Fellowship at Duke University and graduated Summa Cum Laude from Pennsylvania State University. He earned his medical degree from Jefferson Medical College, where he was elected to Phi Beta Kappa and Alpha Omega Alpha. Dr Moul currently serves on the editorial boards of Prostate Cancer, Prostate Cancer and Prostatic Diseases, BJU International, American Journal of Mens Health, Brazilian Journal of Urology, World Journal of Urology, and Oncology REALTIME. He has published over 500 medical and scientific manuscripts and book chapters and has lectured at national and international meetings. He has appeared on ABC, NBC, CNN, PBS, and other media as a prostate cancer authority. Honors and awards received have included the American Medical Associations Young Physicians Section Community Service Award for his national involvement in prostate cancer patient support groups, the Sir Henry Welcome Research Medal and Prize from the Association of Military Surgeons of the United States, the prestigious Gold Cystoscope Award by the American Urological Association, the Baron Dominique Jean Larrey Military Surgeon Award for Excellence, the Order of Military Medical Merit from the Surgeon General at the US Army, and the Castle Connolly National Physician of the Year award.

Professor Howard Morris is Professor of Medical Sciences at the University of South Australia and a Chief Medical Scientist in Chemical Pathology at SA Pathology, Adelaide, South Australia.
He is currently Vice-President of the International Federation of Clinical Chemistry
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and Laboratory Medicine (IFCC) and Chair of the IFCC-International Osteoporosis Foundation Working Group on Standardization of Bone Marker Assays. He has over 30 years experience in Clinical Biochemistry largely managing the Endocrinology laboratory of a large public pathology service. Between 2003 and 2009 he was the Director of the Hanson Institute in Adelaide, the major medical research institute in South Australia. His research investigates the pathophysiology of osteoporosis and the effects of hormones including vitamin D and dietary calcium. He was the Louis Avioli Memorial Lecturer at the 2009 Annual Scientific Meeting of the American Society for Bone and Mineral Research. He is also Chair of the South Australian Department of Health Working Party on Osteoporosis and Fracture Prevention.

Since June 2011, Dr. Harris has served as the Senior Vice President of Translational Medicine at Biogen Idec. Dr. Harris has served as the Director of the Advanced Technology Program at SAIC Frederick since 2007 and Chief Technology Officer for SAIC Frederick since 2008. Prior to
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holding these positions, he served as the President and Chief Executive Officer of Novasite Pharmaceuticals Inc. from January 2005 to September 2006. Prior to that, he served as Chief Executive Officer for Structural GenomiX, Inc., a drug discovery and development company focused on innovative cancer therapeutics from 2003 to 2004 and as its President and Chief Executive Officer from 1999 to 2003. Dr. Harris started his career in biotechnology in 1981 as a group leader in Molecular Biology at Celltech Group and from 1989 to 1993 was Director of Biotechnology at Glaxo Group Research in the U.K. From 1993 until 1999, Dr. Harris was Chief Scientific Officer and Vice President of Research and Development at Sequana Therapeutics Inc. in San Diego, which became Axys Pharmaceuticals, Inc. in 1998 and was subsequently acquired by Celera Genomics. During the past five years, Dr. Harris has served on the board of directors of Dendreon Corporationration and he currently serves on the boards of directors of Origen Therapeutics, Inc. and Gyrasol Technologies and is Chairman of the Scientific Advisory Board of Bionomics Inc. in Australia.

Dr. Geaghan is Chief, Pathology at Lucile Packard Children's Hospital at Stanford, and Co-Director of Clinical Laboratories at Stanford Hospital and Clinics. She also directs the Bass Pediatric Cancer Center Laboratory at the Lucile Packard Hospital; is Director of the Point of
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Care Testing Program for the women and children's hospital and is Director of Stanford Clinical Laboratory at Mary L. Johnson Pediatric Ambulatory Care Center. She is an Associate Professor in the Department of Pathology and in Pediatrics at Stanford University School of Medicine, teaching medical students, residents, fellows and post-graduate continuing medical education programs.
Dr. Geaghan received her undergraduate degree at Dartmouth College and MD at Boston University School of Medicine. She received her training, including two residencies in Anatomic and Surgical Pathology and in Laboratory Medicine, at the University of California, San Francisco, where she also served as Chief Resident and was the first Hematopathology Fellow. Dr. Geaghan holds four board certifications: in Anatomic Pathology; Hematopathology; Clinical Pathology and Pediatric Pathology.
Dr. Geaghan is Chair-elect of the American Association of Clinical Chemistry Division of Pediatric Maternal Fetal Division, the largest organization of laboratory medicine professionals (2012-2014). Dr. Geaghan was recently named to the International Federation of Clinical Chemistry's Task Force on Pediatric Laboratory Medicine, and the College of American Pathologists Point of Care Testing Committee.
Dr. Geaghan serves on numerous Executive Boards, including the Medical Executive Board at Lucile Salter Packard Children's Hospital at Stanford and also serves on Advisory Boards as an avid advocate for children's health, in various national Pediatric Clinical and Laboratory Medicine Associations. She has recently been named in Top Doctors of the Year by San Jose Magazine, and in the American Registry of Outstanding Professionals.

Dr. Willerth currently holds a Canada Research Chair in Biomedical Engineering at the University of Victoria where she is dually appointed in the Department of Mechanical Engineering and Division of Medical Sciences. Her research group investigates how to engineer neural tissue
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by combining pluripotent stem cells, controlled drug delivery and biomaterial scaffolds . She has given invited talks at the Till and McCulloch Annual Meeting and at the 1st Annual British Columbia Stem Cell and Regeneration Medicine Initiative Meeting as well as presented at the 9th Annual World Biomaterials Congress in Chengdu, China. She belongs to both the Brain Research Centre (BRC) and the International Collaboration on Repair Discoveries (ICORD) - B.C. based organizations committed to treating brain diseases and disorders and finding long term treatments for the repair of spinal cord injuries respectively. Before accepting her faculty position, Dr. Willerth completed an NIH post doctoral fellowship at the University of California-Berkeley and graduate studies at Washington University.

Dr. Katerina Venderova obtained her master's and doctorate degrees in pharmacy, and her PhD in Toxicology from Charles University in the Czech Republic. She then received a fellowship from the Parkinson Society Canada and pursued her postdoctoral training at Toronto Western
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Research Institute (2 years), and subsequently at University of Ottawa in Canada (5 years), where she studied genetics of Parkinson's disease, mechanisms of neuronal death and cell signaling in the basal ganglia. Dr. Venderova joined Pacific in 2011.

Ahmad Salehi, M.D., Ph.D. is a Clinical Associate Professor at the Department of Psychiatry and Behavioral Sciences, Stanford Medical School and the Director of the Translational Laboratory at the VA Palo Alto Health Care System in California. He obtained his MD in Tehran, Iran
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and then moved to the Netherlands Institute for Brain Research, in Amsterdam to get his PhD. While he was there, he was selected as the best junior scientist in the field of Alzheimers disease in the Netherlands. After finishing his graduate studies and 3 years of postdoc in Amsterdam, he moved to Stanford Medical School. First as a postdoc, and then as a Senior Research Associate, he worked on mechanisms of failed axonal transport in mouse models of Down syndrome. For almost a decade, he was the Director of Stanford Brain Bank. Since 2009, Dr. Salehi has moved to the Department of Psychiatry and Behavioral Sciences at Stanford. In December 2010, he received the World Technology Award in the field of Biotechnology for his innovative work on the use of mouse models of Down syndrome. During his carrier, Ahmad has been involved in publication of a large number of papers from which several have appeared on the cover of Science, Cell: Stem Cell, Science Translational Medicine, Neuroscience and Bio-behavior Reviews, and Biological Psychiatry (twice).

Dr. Paul J. Mathews received his bachelors degree from the University of Oregon where he studied invertebrate behavioral plasticity in the lab of Dr. Nathan Tublitz. He received his Ph.D. in neuroscience from the University of Texas at Austin under the mentorship of Dr. Nace
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Golding. Dr. Mathews work focused on understanding how the biophysical properties of specific voltage-gated ion channels in an auditory brainstem nuclei contribute to their capacity to make sub-millisecond computations necessary for low frequency sound localization. For the past several years Dr. Mathews has been working at UCLA under the mentorship of Dr. Tom Otis where he is currently working to uncover the cerebellar circuit mechanisms that underlie motor learning and memory. To do this Dr. Mathews is utilizing a multifaceted approach that includes both in vitro and in vivo electrophysiology, optogenetics, advanced optics, histology, and behavioral manipulations to make links between cerebellar circuit activity and motor output in rodent models. He is currently on the job market looking for a tenured track assistant professor position.

Dr. Ulrich Hengst studied biochemistry at the Ruhr University Bochum, Germany, and conducted his graduate research at the Friedrich Miescher Institute for Biomedical Research in Basel, Switzerland, in the group of Prof. Denis Monard. In 2003 he received his PhD from the
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University of Basel. For his postdoctoral training, Dr. Hengst joined the laboratory of Samie R. Jaffrey, MD, PhD at the Weill Cornell Medical College in New York, NY. In Dr. Jaffreys group, he investigated the role of axonally localized mRNAs for axonal development leading to the identification of the first examples of specific mRNAs that are translated in axons in response to extracellular signaling molecules and that mediate growth cone collapse and axon elongation, respectively.
In 2009, Dr. Hengst joined the Department of Pathology and Cell Biology and the Taub Institute for Research on Alzheimers Disease and the Aging Brain at Columbia University Medical Center in New York, NY, as an Assistant Professor. He has successfully established new research projects addressing the role of local protein synthesis in Alzheimers disease and neurodevelopment.

Dr. Anthony A. Grace is a Distinguished Professor of Neuroscience and a Professor of Psychiatry and Psychology at the University of Pittsburgh in Pittsburgh, PA. He received his Ph.D. from Yale University School of Medicine with Dr. Benjamin S. Bunney and had postdoctoral
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training with Dr. Rodolfo Llinas in the Department of Physiology and Biophysics at New York University School of Medicine. Dr. Grace has been involved in translational research related to the dopamine system for over 30 years. His early work pioneered the mode of action of antipsychotic drugs, and the identification and characterization of dopamine-containing neurons, and was the first to provide a means to quantify their activity state and pattern in a way that is the standard in the literature. His current work involves novel treatments for schizophrenia and its prevention, the role of dopamine in anhedonia and affective disorders, and the mode of action of ketamine and novel antidepressant drugs. Dr. Grace has received several awards for his research, including the Paul Janssen Schizophrenia Research Award and the Lilly Basic Scientist Award from the International College of Neuropsychopharmacology, the Efron Award from the American College of Neuropsychopharmacology, as well as a NIMH MERIT award, a Distinguished Investigator Award from the National Alliance for Research in Schizophrenia and Depression, the Judith Silver Memorial Investigator Award from the National Alliance for the Mentally Ill, a Fellow of the American Association for the Advancement of Science, and appointment as a Distinguished Professor of Neuroscience at the University of Pittsburgh. He is also a past member of the governing council of the American College of Neuropsychopharmacology and is on the editorial board for numerous leading journals in the field.

Pierre-Antoine Gourraud is a former student of the Ecole Normale Suprieure de Lyon in France. After receiving an M.P.H. from University Paris XIII in 2002, he got his Ph.D. in Immunogenetic Epidemiology and Public Health from Toulouse University in 2005. He relocated to the
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United States to do his postdoctoral research in Neuroimmunogenetics of multiple sclerosis at UCSF in 2009 and joined the UCSF faculty in 2011. Dr Gourraud has established numerous research collaborations with investigators from all over the world: He develops bioinformatics resources at the National Center for Biotechnology Information (Immunogenetics markers: HLA, KIR, Microsatellites). At UCSF, he performs new generation of MS genetic association studies using massive sequencing technologies in various genetic ancestry backgrounds and continues developing software dedicated to translational digital medicine. His recent efforts have focused on the MS Bioscreen, a tablet-based navigation-system that integrates multiple dimensions of patient information including clinical evolution, therapeutic treatments, brain imaging, genomics and biomarker data.

Dr. Szczepan Baran is the Global Head, Animal Welfare and Compliance Training at Novartis Institutes for Biomedical Research.
Dr. Baran received a Bachelor of Science in Pre-Veterinary Medicine from the University of Delaware, a Veterinary Medical Doctoral degree from the
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University of Pennsylvania School of Veterinary Medicine and a Master of Science in Comparative Medicine from the University Of Washington School Of Medicine.
In 2005, he joined Fred Hutch Cancer Research Center where he was a member of the team that discovered the first canine embryonic stem cells. Then in 2007 Dr. Baran founded and became COO of the Veterinary Bioscience Institute before his current employment at Novartis.
Dr. Baran founded the LinkedIn group "Laboratory Animal Science and Medicine," the largest group in this field. He also served as, Graduate Course Director, Drexel University College of Medicine, Assistant Professor at Delaware Valley, Adjunct Assistant Professor, Department of Pathology, Wake Forest School of Medicine and most notably as Director at Large for the Academy of Surgical Research as well as a Board Member of Americans for Medical Progress.
His research interests include use of microfluidics in safety pharmacology and toxicology, the development and validation of online surgical training programs, and the development and validation of rodent endoscopic procedures. Dr. Baran's hobbies include boxing, micro-facial expressions and psychology of adolescent communication.

Dr. Ottavio Arancio received his Ph.D and M.D. from the University of Pisa (Italy). From 1981 to 1986 he took residency training in Neurology at the University of Verona (Italy). Dr. Arancio has held Faculty appointments at Columbia University, NYU School of Medicine and at
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SUNY HSCB. In 2004 he became Faculty member of the Dept of Pathology & Cell biology and The Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University. His honors include the "G. Moruzzi Fellowship" (Georgetown University), the "Anna Villa Rusconi Foundation Prize" (Italy), the "INSERM Poste vert Fellowship" (France), the AHAF centennial Award (2007), the Zenith Award (2007), the Margaret Cahn Research Award (2008), and the Edward N. and Della L. Thome Memorial Foundation Award.
Dr Arancio is a cellular neurobiologist who has contributed to the characterization of the mechanisms of learning in both normal conditions and during neurodegenerative diseases. During the last ten years he has pioneered the field of mechanisms of synaptic dysfunction in Alzheimer's disease. Dr. Arancio's laboratory has focused primarily on events triggered by amyloid protein. These studies, which have suggested new links between synaptic dysfunction and amyloid protein, are of a general relevance to the field of Alzheimer's disease both for understanding the etiopathogenesis of the disease and for developing therapies aiming to improve the cognitive symptoms.

Dr. Aguilar obtained his PhD degree in Immunochemistry from the School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina. Dr. Aguilar pursued his post-doctoral training at the National institutes of Health in Bethesda, MD in the lab of the well-known cell
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biologist Dr. Juan Bonifacino. In 2005, after a period as Associate Research Scientist at The Johns Hopkins University (in Dr. Beverly Wendland lab), Dr. Aguilar joined the Faculty of the Department of Biological Sciences at Purdue University. There, his group studies the mechanisms linking endocytosis and signaling in health and disease. In order to pursue its research goals, the Aguilar lab routinely use biophysical, biochemical and genetic approaches.

Dr. Antonio T. Baines is an Associate Professor in the Department of Biology at North Carolina Central University (NCCU) and an adjunct professor in the Department of Pharmacology in the School of Medicine at the University of North Carolina (UNC) Chapel Hill. He earned a
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bachelors degree in biology from Norfolk State University and a doctorate in pharmacology and toxicology from the University of Arizona. Afterwards, Dr. Baines accepted a postdoctoral fellowship at UNC in pharmacology and radiation oncology under Drs. Channing Der and Adrienne Cox. His research focused on understanding the role of the Ras oncogene as a molecular target in pancreatic cancer oncogenesis. In August 2006, Dr. Baines accepted a tenure-track faculty position at NCCU where he currently teaches and conducts research as a cancer biologist. Also, he mentors high school, undergraduate, and graduate students in his laboratory. Pancreatic cancer is the 4th most common cause of cancer deaths in the United States with a high mortality rate and very limited treatment options. The overall focus of Dr. Baines research program is to identify and validate novel molecular targets in pancreatic cancer which can be targeted by potential cancer therapeutics. Additionally, his lab aims to understand the role of these molecular targets in the development and progression of normal cells transforming into cancer cells of the pancreas. Currently, Dr Baines studies the functional significance of the oncogenic Pim kinase family in pancreatic cancer growth and development. He hypothesizes that inhibition of these enzymes will be an effective approach for antagonizing the aberrant growth of pancreatic carcinoma. In addition to working with colleagues in academia, he collaborates with various pharmaceutical companies that are developing Pim inhibitors. Results from his studies will allow for critical validation of these kinases as novel therapeutic targets for pancreatic cancer treatment. Dr. Baines research has been funded by NIH and other grant sources. He has presented his research at various national scientific meetings such as the Society of Toxicology and the American Association for Cancer Research. In addition, Dr. Baines has given invited research seminars at universities such as Duke University, UNC-Chapel Hill, North Carolina Agricultural and Technical (A&T) State University, Indiana University, North Carolina State University, University of Missouri-Kansas City and Massachusetts Institute of Technology (MIT).

Dr. Bayrak-Toydemir is the medical director of the Molecular Genetics and Genomics Laboratories at ARUP and an associate professor of pathology at the University of Utah School of Medicine. Dr. Bayrak-Toydemir received her MD from the Ankara University School of Medicine in
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Ankara, Turkey, where she also received her PhD in human genetics. Subsequently, she completed her fellowship in clinical molecular genetics at the University of Utah. She is board certified in medical genetics.
Dr. Bayrak-Toydemir has focused her research efforts on understanding the molecular genetic characteristics of the Hereditary Hemorrhagic Telangiectasia (HHT) disease, an autosomal dominant vascular dysplasia. Her research aims to identify additional gene(s) that can cause HHT disease, to determine the roles of regulatory region mutations of known HHT genes, and to describe the genotype-phenotype correlation. In addition to HHT, her research aims to identify gene(s) that cause various inherited vascular malformations. She is also interested in application of next generation sequencing to molecular diagnostics.

Director, Clinical Chemistry Laboratory University Hospital Director, General Laboratory Cancer Treatment Research Center Director, Proteomics Laboratory UTHSC at San Antonio Interim Director, Molecular Laboratory UTHSC at San Antonio Associate Director, Mycology Laboratory UTHSC
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at San Antonio I graduated from the Collegium Medicum at Jagiellonski University in Poland, and subsequently completed residency program in anatomic, clinical pathology and clinical chemistry. I have been practicing pathology in the University of Texas Health Science Center at San Antonio, Texas as a staff pathologist and medical director of clinical chemistry and molecular laboratory. I have been serving the Instrumental Resource Committee of the College of American Pathologist (CAP) since 2008. Since 2009 I have served for the Pharmacogenomics Committee, Educational subcommittee working on Pharmacogenomics Educational Course. I was actively involved in the CLSI on a project "Method Validation by using patient's sample". The main scientific interest is in biomarkers for aggressive prostate cancer as well as biomarkers for monitoring the trauma patients with hemorrhagic shock.

George Fritsma is an associate professor in Laboratory Medicine of the Department of Pathology at the University of Alabama at Birmingham.
Prof. Fritsma manages www.fritsmafactor.com, "The Fritsma Factor, Your Interactive Hemostasis Resource," a clinical coagulation
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educational resource and blog. The Fritsma Factor is sponsored by Precision BioLogic, Inc, Dartmouth, Nova Scotia, Canada.
Prof. Fritsma is the continuing education editor for the Clinical Laboratory Science Journal and a member of the American Association for Clinical Chemistry publications committee. He is co-editor of Hematology Clinical Principles and Applications, 4th edition, 2012, and he is and co-author of Quick Guide to Renal Disease Testing, 2011; Quick Guide to Venipuncture, 2010; Quick Guide to Coagulation 2nd Edition, 2009; and Quick Guide to Hematology Testing, 2007, all available from the ASCLS bookstore.
Prof. Fritsma is a 40-year member of the American Society for Clinical Laboratory Science and a member of the International Society for Thrombosis and Haemostasis. He holds a bachelor's degree in biology and chemistry from Calvin College, Grand Rapids, Michigan, a Masters in Medical Technology from Wayne State University, Detroit, and advanced course work from the University of Illinois at Chicago.

Bradley Ford received his M.D. and Ph.D. (Physiology and Biophysics) degrees from SUNY Stony Brook, followed by a Clinical Pathology residency and postdoctoral training in basic and clinical microbiology at Washington University in St. Louis. His research interests include
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bacterial pathogenesis and application of biophysical and computational methods to improve clinical diagnostics.

Dr. Charles Cantor is a founder, and Chief Scientific Officer at SEQUENOM, Inc., which is a genetics discovery company with tools, information and strategies for determining the medical impact of genes and genetic variations.
He is also the founder of SelectX Pharmaceuticals
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a drug discovery company, Retrotope, an anti-aging company, and DiThera, a biotherapeutic company.
Dr. Cantor is professor emeritus of Biomedical Engineering and of Pharmacology and was the director of the Center for Advanced Biotechnology at Boston University. He is currently adjunct professor of Bioengineering at UC San Diego, adjunct professor of Molecular Biology at the Scripps Institute for Research, and distinguished adjunct professor of Physiology and Biophysics at UC Irvine. Prior to this, Dr. Cantor held positions in Chemistry and then in Genetics and Development at Columbia University and in Molecular Biology at the University of California at Berkeley. Cantor was educated in chemistry at Columbia College (AB) and at the University of California Berkeley (PhD).
Dr. Cantor has been granted more than 60 US patents and, with Paul Schimmel, wrote a three-volume textbook on biophysical chemistry. He also co-authored the first textbook on Genomics titled 'The Science and Technology of the Human Genome Project'. In addition, he sits on the advisory boards of numerous national and international biotechnology firms, has published more than 450 peer-reviewed articles, and is a member of the U.S. National Academy of Sciences.

Dr. Cynthia Bowman has been a broad based general pathologist for over 30 years. She graduated with a BA in Chemistry from St. Olaf College, received her MD from Vanderbilt University Medical School, and trained for 6 years at the University of California, San Francisco as a
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surgery intern and then anatomic and clinical pathology resident. She worked as an emergency room physician during training and has always had a clinical perspective in her practices. She has worked in California, Maine, Massachusetts, New York and Australia as an anatomic and clinical pathologist and laboratory medical director in small, mid-sized, tertiary and academic medical centers. She is currently Medical Director at Enzo Clinical Laboratories, a commercial reference laboratory and bioscience company in the NY metropolitan area, and in that capacity collaborates with the development and integration of molecular services into clinical testing. She has been active in national laboratory organizations, especially the College of American Pathologists, where she was chair of the Point of Care Testing Resource Committee. In that capacity she guided the introduction and was the senior editor of a web-based POCT toolkit as a resource for laboratory director leadership in POCT. She has also written and edited multiple educational pieces for the laboratory community as part of the CAP Excel Survey program and in 2012 she was awarded a Life Time Achievement Award by the CAP. She has spoken at AACC and CAP meetings and currently serves on several CLSI document development committees. She is currently chair of an International Federation of Clinical Chemistry POCT task force work group addressing the use of glucose meters in critical care patients. Her professional commitment has always been to integrate and translate pathology and laboratory medicine services into effective clinical care. She has dedicated her efforts in POCT as part of that vision to collaborate with all stakeholders and involve laboratory services as part of the continuum of care. She enjoys evaluating technology and integrating it into laboratory services.

Dr. Borchers received his B.S., M.S. and Ph.D. from the University of Konstanz, Germany. After his post-doctoral training and employment as a staff scientist at NIEHS/NIH/RTP, NC and he was the director of the Duke - UNC Proteomics Facility and held a faculty position at UNC
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Medical School in Chapel Hill, NC (2001-2006). Since then Dr. Borchers is Associate Professor at University of Victoria (UVic), Canada and the Director of the UVic - Genome Proteomics Centre. His research is centred around the improvement, development and application of proteomics technologies with major focus on techniques for quantitative targeted proteomics for clinical diagnostics.

Dr. Peter Blume-Jensen has extensive expertise in basic and translational cancer research, oncogenic signaling, and targeted oncology therapeutics drug discovery prior to joining Metamark as CSO in 2010.&nbsp; From 2001 to 2008 Peter was department head at first Serono, US and
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later at Merck Research Laboratories, Merck &amp; Co, Inc. where he established novel, integrated oncology drug discovery departments and programs linking therapeutics to patient responder populations. During his tenure he advanced a number of pre-clinical drug programs into the clinic, and provided translational support for clinical programs. Since 2008 he was Exec. Dir. and Vice President for External Scientific Affairs at Daiichi Sankyo Inc., served as the global 'Therapeutic Area Advisor' for Oncology, and was co-responsible for formulating a global oncology R&amp;D strategy. He co-led the scientific M&amp;A and due diligence resulting in the acquisition of Plexxikon (US$935M).&nbsp; In 2010 he joined Metamark as CSO and 2nd employee.&nbsp; Here he built and let R&amp;D, a world-class KOL Advisory Board, and a novel, automated proteomics imaging platform for CLIA-certified cancer tests.&nbsp; He designed and let 4 clinical studies culminating with the successful blinded, clinical validation of ProMark, a prognostic prostate cancer biopsy test for intact tissue.&nbsp; During the initial commercial launch in Q1-2, 2014 he led Medical Affairs and training of all commercial staff.&nbsp; Since June 2014, Peter has joined Xtuit Pharmaceuticals, a targeted therapeutics start-up, as CSO, and first employee.&nbsp; Peter continues to serve as Chief Scientific Advisor and on the SAB for Metamark and also has joined the SAB of Veritas Gene, Inc, a NGS company. <br /> <br />Dr. Blume-Jensen has authored highly-cited original articles, reviews, and book chapters in Personalized Molecular Oncology. His review 'Oncogenic Kinase Signaling' in Nature is a citation classic in 'Clinical Medicine', and his work on genetically engineered cancer and male infertility mouse models has been widely portrayed on CNN and other news channels. His approaches for efficacy-predictive biomarkers have appeared on Nature Biotechnology's 'Hot patents' watch-list and in numerous Editorial highlights for Personalized Oncology. Dr. Blume-Jensen obtained his M.D. from Copenhagen, Denmark, his Ph.D. from Dr. Carl-Henrik Heldin's laboratory at the Ludwig Institute for Cancer Research, Uppsala, Sweden, and conducted his Post-Doctoral studies in Dr. Tony Hunter's laboratory at the Salk Institute, La Jolla, CA. He has consulted extensively for Biotech and Pharma on targeted therapeutics and Precision Medicine

Dr. Blonder leads the Clinical Proteomics Group at the CRTP/FNL. FNL is a Federally Funded Research and Development Center operated by Leidos Biomedical Research, Inc., for the National Cancer Institute (NCI). In 1978, Dr. Blonder received his M.D. at the Rijeka University
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School of Medicine, Croatia. In 2000, through Associated Western Universities, Dr. Blonder was awarded a post-doc fellowship in proteomics at the Pacific Northwest National Laboratory (PNNL), Richland, WA (Advisor: Dr. Richard D. Smith). At the PNNL, his research was focused on studying cell surface proteins using mass spectrometry (MS)-based proteomics. In 2002, Dr. Blonder joined FNL (formerly NCI-Frederick) where he continues to develop and apply MS-based proteomics to cancer research. Since 2006, he has led the Clinical Proteomics Group, extending his research on development of shotgun proteomics for in-depth profiling of membrane proteins found at the cell surface of cancer cells. In parallel, he worked on methodology for cancer biomarker and drug target discovery using precision proteomics for targeted profiling of clinical tissue and blood specimens. His group was the first to optimize the immunodepletion of abundant proteins from clinical tissue homogenates. Currently, Dr. Blonder is leading the effort towards molecular mapping of the KRAS cell surface as a part the RAS program. This program is spearheaded by the FNL as a national mission to attack RAS-driven cancers. Dr. Blonder brings unique combination of his expertise in medicine, clinical proteomics, and pathway analysis, focusing his research on the development of innovative approaches for molecular profiling of cancer cell lines, body fluids and tissue specimens. He is an editor of BMC Cancer and a lecturer at the Foundation for Advanced Education in the Sciences at NIH. Since 2002, Dr. Blonder has authored over 50 scientific publications in areas of biological mass spectrometry, clinical proteomics and cancer research.